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Biomedical subjects

R L Feldman

Publications and source records attributed to R L Feldman.

At least 55 records · Page 3Linked to original sources
PubMed1986

Percutaneous transluminal coronary angioplasty in evolving acute myocardial infarction.

In 29 patients with evolving acute myocardial infarction, acute reperfusion of the infarct-related coronary artery was attempted using percutaneous transluminal coronary angioplasty (PTCA). Before PTCA, angiography showed 23 totally occluded and 6 severely stenotic infarct-related coronary arteries. PTCA was initially successful in 25 of 29 patients (86%). Reocclusion occurred in 4 patients within 12 hours after successful PTCA and was associated with new electrocardiographic changes or recurrence of symptoms. In 17 patients the infarct-related coronary artery remained patent at early follow-up; late stenosis occurred in 4 patients. Recurrence of stenosis was accompanied by development of angina. No clinical or angiographic features distinguished those with ultimate vessel patency, occlusion or recurrence of stenosis. On follow-up, ventricular function appeared better preserved or improved in those with a patent infarct-related coronary artery than in those with an occluded infarct-related coronary artery. Further studies are warranted to compare PTCA and streptokinase as primary reperfusion modalities in evolving acute myocardial infarction.

Adult↗
PubMed1986

Effects of diltiazem during tachycardia-induced angina pectoris.

To investigate the mechanism of relief of angina pectoris by diltiazem administration, 14 patients with effort angina were studied using a protocol to control heart rate. Coronary, systemic and left ventricular (LV) hemodynamic function was assessed at rest and during tachycardia stress (atrial pacing)-induced angina before and during diltiazem infusion. Angina occurred in all patients during tachycardia stress before diltiazem administration. During tachycardia stress at the heart rate that produced angina after diltiazem infusion, pressure-rate product, coronary sinus flow and resistance and ST-segment depression were all similar to findings before diltiazem. Although at the onset of angina, systolic pressure was usually slightly lower after diltiazem infusion (138 +/- 11 vs 128 +/- 11 mm Hg, p less than 0.05), the pacing rate at onset of angina was higher in only 3 patients and the pressure-rate product was higher in only 1 patient. After diltiazem, left ventricular end-diastolic pressure increased less frequently after interruption of pacing. The results suggest that diltiazem favorably alters the relation between myocardial oxygen demand and supply at rest, but during tachycardia, anginal threshold and coronary reserve do not change. Diltiazem's potent antianginal action, shown in previous investigations using exercise-induced angina, is not prominent when heart rate is controlled. The major benefit of diltiazem in patients with stress-induced angina is related to reduction of myocardial oxygen demand rather than improved myocardial oxygen delivery.

Adult↗
PubMed1986

Coronary angioplasty at the time of initial cardiac catheterization.

Following initial diagnostic cardiac catheterization in 20 patients with unstable angina, percutaneous transluminal angioplasty (PTCA) was successfully performed either immediately (15 patients) or later in the day (five patients). This approach offers certain clinical and financial advantages. PTCA immediately following diagnostic catheterization should probably only be performed by experienced operators and only when excellent cooperation with cardiovascular surgeons is possible.

Adult↗
PubMed1986

Salvage coronary angioplasty for symptoms refractory to medical therapy.

Coronary angioplasty was used without surgical back-up in eight patients with angina refractory to medical therapy. After careful evaluation, none of these patients was felt to be a candidate for elective or emergent bypass surgery. Angioplasty provided a reasonable means of coronary revascularization. In each patient, extenuating clinical circumstances and reduced left ventricular function led to this approach. Angioplasty was angiographically and clinically successful in each patient.

Aged↗
PubMed1986

Pharmacodynamic aspects of intravenous diltiazem administration.

The diltiazem serum concentration and the magnitude and time course of systemic and coronary hemodynamic and ECG responses to intravenous diltiazem (250 micrograms/kg intravenous bolus plus 1.4 micrograms/kg/min infusion) were investigated in 14 patients with chronic stable angina pectoris. After 3, 8, and 15 minutes this dosing schedule produced serum concentrations of 570 +/- 259, 199 +/- 62, and 136 +/- 30 ng/ml, respectively (mean +/- SD). These drug levels were associated with a small, transient increase in heart rate (6 bpm, mean) at 3 minutes, which occurred during the nadir of the blood pressure response. But at 8 and 15 minutes, heart rate was unchanged compared to control rates, although blood pressure remained decreased (19%, p less than 0.01 at 15 minutes). Pressure-rate product was significantly reduced as left ventricular end-diastolic pressure and dP/dT remained unchanged. Systemic resistance decreased 17% (p less than 0.05) and stroke index increased 10% (p less than 0.01). Coronary flow was maintained as coronary resistance declined (14%, p less than 0.01). PR interval prolongation (14%, p less than 0.01) occurred at 15 minutes. Correlations between changes in systolic, diastolic, and mean pressures and drug concentration were significant (r = -0.59, -0.80, and -0.78, respectively, all p less than 0.05). The intercept for each regression line was approximately 96 ng/ml diltiazem concentration, suggesting that this represents the minimum effective diltiazem serum concentration. These results indicate that intravenous diltiazem is well tolerated and promptly reduces blood pressure and both systemic and coronary resistances without oxygen-wasting effects of an increase in heart rate.

Adult↗
PubMed1986

Effects of nicardipine on left ventricular function and energetics in man.

The effects of nicardipine, a new dihydropyridine calcium antagonist, on left ventricular function and energetics were studied in 13 patients. Nicardipine was administered as a 2 mg bolus (i.v.) followed by an infusion titrated to maintain a 10-20 mm Hg decrease in systolic pressure. Nicardipine increased heart rate 19% (P less than 0.001) while left ventricular end-diastolic pressure was not significantly changed and stroke volume (ml) increased 13% (P less than 0.01). Peak values for the first and second time derivatives of left ventricular pressure were increased by 26% (P less than 0.01) and 50% (P less than 0.02) respectively. Peak aortic blood flow, peak aortic blood acceleration, and the peak rate of change of ejection power were increased 86% (P less than 0.001), 123% (P less than 0.01), and 113% (P less than 0.001), respectively. Stroke work was not changed during nicardipine infusion. External power increased by 40% (P less than 0.01); however, the ratio of oscillatory to total power was not significantly different. Although the product of heart rate and systolic aortic pressure was not significantly altered with nicardipine, myocardial oxygen consumption increased 18% (P less than 0.02) with a disproportionate increase in coronary blood flow of 41% (P less than 0.001) and decrease in coronary resistance of 39% (P less than 0.001). The time constant for left ventricular isovolumic relaxation decreased 22% (P less than 0.001) during nicardipine infusion while the minimum value of dP/dt was unchanged. Thus, when administered intravenously in man, nicardipine is a potent coronary and systemic vasodilator producing reflex tachycardia, increased indices of myocardial contractile state, and improved isovolumic relaxation with an associated increase in myocardial oxygen consumption.

Angina Pectoris↗
PubMed1986

Effect of propranolol on myocardial ischemia occurring during acute coronary occlusion.

In 16 patients undergoing angioplasty of the left anterior descending coronary artery, the clinical, electrocardiographic, and hemodynamic effects of short-term intravenous nonselective beta-adrenergic blockade with propranolol (0.1 mg/kg) were assessed during temporary occlusion of the artery. Myocardial ischemia during coronary occlusion was prevented, delayed in onset, or diminished in magnitude by propranolol in 10 of the 16 patients. Propranolol decreased values for indexes of myocardial oxygen demand, such as heart rate and blood pressure and their product, in all patients. Surprisingly, in patients who derived clinical benefit, propranolol did not change indexes of myocardial oxygen supply to the left ventricular region perfused by the occluded artery. For example, great cardiac vein flow (40 +/- 15 to 41 +/- 17 ml/min, p = NS) and coronary collateral resistance (2.1 +/- 1.0 to 2.1 +/- 1.1 mm Hg/ml/min, p = NS) were unchanged. In contrast, a worsening of supply occurred in patients who were not benefited: great cardiac vein flow (50 +/- 10 to 39 +/- 6 ml/min, p less than .05) decreased and coronary collateral resistance (1.6 +/- 0.5 to 2.0 +/- 0.6 mm Hg/ml/min, p less than .05) increased. Information obtained from this study demonstrates the value of this new experimental preparation in helping assess potential clinical effectiveness of drug interventions during the initial phase of acute coronary occlusion and providing insight into the mechanisms of drug effect.

Adult↗
PubMed1986

ST segment response to acute coronary occlusion: coronary hemodynamic and angiographic determinants of direction of ST segment shift.

To assess the relationship between the direction of ST segment response to transient coronary occlusion and collateral function, we studied 25 patients with diagnostic ST segment changes during transient occlusion of the proximal left anterior descending artery (LAD). Electrocardiographic leads I, II, V2, and V5; left ventricular filling, aortic, and distal coronary pressures; and great cardiac vein flow were measured during percutaneous transluminal coronary angioplasty (PTCA) of the LAD. During a 1 min LAD balloon occlusion, 16 patients had reversible ST elevation (group I) and nine patients had ST depression (group II). The ST responses in individual patients were consistent during repeated occlusions, and ST depression never preceded ST elevation. Angiography before PTCA showed less severe LAD stenosis in group I (69 +/- 15%) than in group II (88 +/- 10%; p less than .01) and collateral filling of the LAD in no group I patient but in six of nine patients in group II (p less than .01). During LAD occlusion, determinants of myocardial oxygen demand (left ventricular filling pressure, aortic pressure, heart rate, and double product) were similar in both groups. Group I patients, however, had lower distal coronary pressure (25 +/- 8 vs 41 +/- 16 mm Hg) and residual great cardiac vein flow (33 +/- 14 vs 51 +/- 22 ml/min) and higher coronary collateral resistance (3.1 +/- 2.1 vs 1.5 +/- 0.8 mm Hg/ml/min) than group II patients (all p less than .05). In patients with ST elevation during LAD occlusion, stenosis before PTCA was less severe, visible collaterals were not present, and hemodynamic variables during LAD occlusion reflected poorer collateral function.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1985

The healing process in normal canine arteries and in atherosclerotic monkey arteries after transluminal laser irradiation.

To evaluate the healing response of both normal and atherosclerotic arteries to laser radiation, 7 mongrel dogs and 4 hypercholesterolemic atherosclerotic monkeys underwent catheterization with a right Judkins catheter-optical fiber system designed to maximize arterial wall injury. Argon laser radiation was then delivered to the abdominal aorta and iliofemoral arteries. In the 11 animals, a total of 917 sites were irradiated in 33 arteries. Angiography did not reveal dissection or aneurysm formation; occlusive thrombosis was found in 2 arteries. Perforation of the arterial wall was a frequent complication. In animals killed between 1 hour and 4 days, light and electron microscopy of lased sites showed craters filled with a coagulum of blood and cellular debris with only a few adherent platelets. Healing occurred with a minimal inflammatory response and involved both fibroblasts and smooth muscle cells. Reendothelialization was seen in all animals killed between 7 and 14 days after lasing and was complete by 30 to 60 days. Within this period, no accelerated atherosclerosis was seen at lased sites in the hypercholesterolemic monkeys. It is concluded that transluminal lasing of normal arteries in dogs and in atherosclerotic arteries of monkeys is followed by healing and reendothelialization within a few weeks.

Angiography↗
PubMed1985

Systemic, left ventricular and coronary hemodynamic effects of intravenous diltiazem in coronary artery disease.

Systemic and coronary hemodynamic effects of intravenous diltiazem, administered as a bolus of 250 micrograms/kg followed by an infusion of 1.4 micrograms/kg/min, were examined in 14 patients with effort angina. There was no change in heart rate despite significant decreases in systolic, diastolic and mean systemic pressures (13%, 10% and 11%, respectively, all p less than 0.01). The blood pressure decrease was closely correlated with the initial blood pressure (r = 0.81, p less than 0.05). Neither left ventricular end-diastolic pressure nor peak dP/dt changed significantly, but peripheral vascular resistance decreased 16% (p less than 0.001) and stroke volume index increased 10% (p less than 0.05). The pressure-rate product decreased 15% (p less than 0.005), but coronary blood flow was maintained as coronary resistance decreased 14% (p less than 0.025). Diltiazem increased regional coronary flow in some patients. Thus, intravenous diltiazem dilates coronary and systemic resistance vessels, without an increase in heart rate, favorably altering indexes of myocardial oxygen supply and demand.

Adult↗
PubMed1985

Nicardipine for angina pectoris at rest and coronary arterial spasm.

The antiischemic effects and safety of nicardipine were assessed in 17 patients with angina at rest and coronary arterial spasm in a randomized placebo-controlled study over 8 to 13 weeks. Eleven patients had previously had unsatisfactory results with long-acting nitrates or other calcium blockers. The average daily dosage of nicardipine for optimal angina relief was 89 mg (range 40 to 160). During the double-blind phase, angina frequency decreased with nicardipine compared with placebo (mean 0.47 vs 2.11 attacks/day, p less than 0.05). A similar decrease in nitroglycerin requirements occurred (0.51 vs 2.77 tablets/day, p less than 0.05). During placebo periods, 51 episodes of ischemic ST-segment shifts occurred during 482 hours of ambulatory electrocardiographic monitoring and 12 (24%) were associated with angina. During nicardipine treatment, only 15 episodes of ST-segment shifts occurred during 498 hours of monitoring. In 1 patient a burning skin rash developed; otherwise, the drug was generally well tolerated. Thus, nicardipine is effective and safe in preventing symptomatic and asymptomatic ischemia in patients with coronary spasm. It may be particularly beneficial in patients with unsatisfactory responses to other therapy.

Aged↗
PubMed1985

Coronary hemodynamic responses during spontaneous angina in patients with and patients without coronary artery spasm.

The mechanisms of spontaneous angina were evaluated during cardiac catheterization in 13 patients who had angina occurring without provocation at rest. Left ventricular and systemic hemodynamics, coronary venous flows (thermodilution technique), electrocardiogram and coronary angiograms were recorded before and during spontaneous angina. Angiography during spontaneous angina showed that 5 patients had coronary spasm (group I) and 8 patients did not (group II). In group II there was a preponderance of multivessel coronary artery disease. Left ventricular end-diastolic pressure increased in all patients in both groups during spontaneous angina. In group I, 4 patients had transient ST elevation and 1 patient had peaked T waves during angina. Transient ST depression occurred during spontaneous angina in all group II patients. Group I patients had decreased coronary sinus flow (4 of 5 patients) or decreased regional flow (5 of 5) during spontaneous angina. Coronary resistance and ratio of double product to coronary blood flow increased in all patients. In group II, coronary hemodynamic responses during spontaneous angina varied. Coronary venous flows, coronary resistance and ratio of double product to coronary blood flow showed no uniform pattern. Thus, patients with severe coronary artery disease can have spontaneous angina without angiographic findings of coronary spasm. After analysis of angiograms and coronary hemodynamics in these patients, no apparent uniform mechanism for spontaneous angina was found.

Aged↗
PubMed1985

Coronary and systemic hemodynamic effects of nicardipine.

Systemic and coronary hemodynamic effects of a new dihydropyridine calcium antagonist, nicardipine, were studied in 15 patients. Nicardipine was administered as a 2-mg bolus intravenously followed by an infusion titrated to maintain a 10 to 20-mm Hg decrease in systolic pressure. Nicardipine increased both heart rate from 69 +/- 3 to 81 +/- 3 beats/min and cardiac output from 7.3 +/- 0.5 to 9.9 +/- 0.5 liters/min (both p less than 0.001) as systemic vascular resistance decreased from 1,183 +/- 70 to 733 +/- 33 dynes s cm-5 (p less than 0.001). Left ventricular end-diastolic pressure remained constant, at 14 +/- 1 vs 14 +/- 1 mm Hg as stroke volume increased from 108 +/- 6 to 123 +/- 6 ml/m2 (p less than 0.001). Coronary blood flow increased from 102 +/- 9 to 147 +/- 13 ml/min, while coronary resistance decreased from 1.17 +/- 0.1 to 0.7 +/- 0.1 mm Hg/ml/min (both p less than 0.001). Heart rate-systolic blood pressure product did not change (104 +/- 5 vs 106 +/- 5 beats/min mm Hg X 10(-2), difference not significant) with drug administration. At the same heart rate before and during nicardipine administration (using atrial pacing in 6 patients), significant augmentation of coronary flow was still observed. Thirteen of 14 patients showed a greater percent decrease in coronary resistance than systemic vascular resistance. Nicardipine differs from other calcium antagonists with respect to consistent augmentation of coronary blood flow. This effect appears to be the result, in part, of increased potency in the coronary bed compared with the systemic vascular bed.

Aged↗
PubMed1985

A modified catheter system for retrograde left ventricular catheterization in aortic valve stenosis.

Conventional retrograde catheterization of the left ventricle using a single large catheter through severely stenotic aortic valves or prostheses has recognized difficulties. An alternative method is described. This method incorporates a coronary angioplasty guide catheter and coronary probing catheter attached to separate pressure transducers allowing simultaneous recording or aortic and LV pressures. This technique was used in seven patients with aortic stenosis in whom a conventional approach had failed. The movable probing catheter permits alterations of the catheter orientation and angulation while the guiding catheter stabilizes the system within the high velocity jet formed in the ascending aorta. This stabilization and the small size of the coronary probing catheter permit exploration of the valve surface and allow for insertion through a tilting disc valve or a severely stenotic valve without significantly altering hemodynamic function. In our laboratory this technique allowed us safely and reliably to assess aortic valve dynamics in each of the patients in whom the technique was attempted without resorting to either transseptal or direct left ventricular puncture.

Aortic Valve Stenosis↗
PubMed1985

Isosorbide dinitrate and nifedipine in variant angina pectoris.

The efficacy of isosorbide dinitrate (ISDN) in variant angina is enhanced by the addition of a calcium antagonist. A prospective double-blind, crossover trial of ISDN, 40 to 120 mg/day, and nifedipine, 40 to 120 mg/day, in 19 patients with variant angina and various degrees of coronary atherosclerosis showed that although both agents were equally effective in controlling angina of vasospastic origin, some patients responded better to one or the other drug. Such response could not be predicted by demographic factors, ECG changes, or degree of coronary atherosclerosis. Since quantitative angiography done in a similar group of patients showed that intracoronary nitroglycerin, 200 micrograms, was a more potent vasodilator than sublingual nifedipine, 10 mg (p less than 0.01), the calcium antagonists may have a different mechanism of preventing variant angina attacks and may act in an additive or synergistic fashion when administered in combination with long-acting nitrates. Such a combination will increase coronary blood flow, reduce ventricular volume and end-diastolic pressure, and reduce systemic arterial resistance. Coronary vasospasm may be directly prevented by a general inhibition of smooth muscle contraction by the calcium antagonist. Clinical studies suggest that combination therapy significantly improves the long-term prognosis of patients with variant angina and reduces the need for bypass surgery. Thus combining ISDN with a calcium antagonist is a rational and effective treatment for variant angina.

Angina Pectoris, Variant↗